cardiac Flashcards
systolic BP
highest pressure achieved by the contraction of the L ventricle
diastolic BP
BP maintained in aorta between ejections
pulse pressure
difference between SBP and DBP
baroreceptors
send signals to brain when there are changes in BP
If there is a change in BP, what happens to the cardiovascular center?
HR increases and it vasoconstricts to increase blood flow to the heart
Neural and Humoral mechanisms are responsible for what type of regulation of BP? what about Renal mechanisms?
Short term, neural: SNS and PNS Humoral: RAA, ADH
renal: long term
stage 1 HTN SBP
140-159
stage 2 HTN SBP
> 160
what is the role of the sympathetic nervous system?
increases contractility and heart rate, induces anteriolar vasoconstriction, contributes to structural remodeling of blood vessels, renal and NA retention
what is the Renin-angiotensin-aldostrone system?
liver produces angiotensinogen which acts on kidneys which produce rennin which makes Agiotensin 1 which goes to lungs which produce ace which makes angiotensin 2 which act on adrenal glands which make aldosterone which increases NA absorption which increases BP, this also causes vasoconstriction in arterioles
Primary HTN
HTN d/t elevation in BP that is not the result of another disease process
Secondary HTN
HTN resulting from another disorder ex. kidney disease, pregnancy
malignant HTN
accelerated form of HTN DBP >120, medical emergency!
you can get cerebral edema and otic nerve swelling, H/A
Isolated Systolic HTN (ISH)
hypertension in elderly d/t stiffened arteries
Oslers maneuver
compress radial artery and if artery is palpable then its not true HTN, its pseudohypertension because arteries are stiff
Target Organ Disease (TOD)
increased workload of L ventricle which leads to heart failure, atherosclerosis develops, decreased GFR of kidneys leads to nocturia, proteninuria
what causes Orthostatic Hypotension
decrease in venous return, decreased cardiac output
conditions that cause orthostatic hypotention
dehydration, bed rest, spinal cord injury, vomiting, diarrhea, medications, autonomic nervous system disorders, aging
Atherosclerosis
hardening of arteries, lesions in arteries
fatty streaks, what is it made up of
common in all ages, contains foam cells of smooth muscle, thin, yellow that progressively enlarge
Fibrous Plaques, what is it made up of and what does it do
connective tissue, progressively thickens and occludes lumen
Complicated lesion, what is it made up of and what does it do
fibrous plaque thats soft that can rupture, contains ulcers that can crack and bleed and the forms a clot!
common sites for atherosclerotic lesion
abdominal aorta and iliac arteries, carotid arteries, thoracic aorta, femoral, popliteal arteries, coronary arteries
Artherosclerotic lesions: Fixed or stable plaque
obstructs blood flow and is implicated in stable angina
Artherosclerotic lesions: unstable or vulnerable plaque
can rupture, cause thrombus formation and is implicated in unstable angina and MI
what determines the vulnerability of plaque in atherosclerosis to rupture?
size, thickness, inflammation, lack of smooth muscle with impaired healing, thin fibrous cap
CAD risk factors
low birth weight, obesity, HTN, hyperlipidemia, smoking, family Hx, men >45, women >55
Hyperlipidema risk factors
cholesterol >200, dietary, genetic,alcoholism, hypothyroidism, corticosteriods, estrogens
Homocysteine
promotes progression of atherosclerosis by causing endothelial damage and increases LDL and smooth muscle growth
who should be screened for high levels of Homocysteine?
unusual family hx, poor nutritional status, unexplained atherosclerosis deposits
major complications of atherosclerosis
Ischemic heart disease, Stroke, PVD
Coronary heart disease: Chronic Ischemic heart disease
chronic stable angina, silent heart ischemia and varient vasospastic angina
Coronary heart disease: Acute coronary syndrome
NSTEMI, STEMI
Coronary Artery Disease
narrowing of the coronary arteries d/t atherosclerosis
Coronary Artery disease affect on the heart and what does it lead to
it blocks the oxygen supply to heart tissue which leads to HTN, angina, hysrhythmias, MIs, CHF
Collateral circulation
growing new vessels to supply organs
what do you see on an EKG with CAD with ischemia? during MI?
ischemia: ST or T wave depression
MI: ST elevation, T wave depression
which hour are you hypercoagulable which leads to the most MIs?
6am
1 Sudden cardiac death cause
because of lethal dysrhythmias
unstable angina and causes
recent onset, change in pattern
causes: atherosclerotic plaque disruption, platelet aggregation, secondary hemostasis
stable angina and causes
constant pattern of pain and severity
causes: coronary stenosis
Variant (Printzmetals angina) and causes
rest pain and V-arrhythmias cause by carotid artery spasm,
causes: drug abusers, coronary vasospasm
Angina heart sounds
split S2 on expiration, S4, S3, systolic murmur
how many days until granulation tissue forms after an AMI?
8-10 days
how long after an AMI does infarct turn gray with yellow streaks?
48 hrs
how long after an AMI does necrotic area develop into a scar?
2-3 months
the size of an AMI depends on what?
extent, severity, duration, amount of collateral circulation, metabolic needs of the heart at the time of the event
anterior or septal MI occurs when which artery is obstructed?
left anterior artery (LAD)
lateral wall MI occurs when which artery is obstructed?
circumflex artery
Inferior/posterior wall MI occurs when which artery is obstructed?
right coronary artery (RCA)
Subendocardial infarcts, what does it involve and when does it occur
involve 1/2 of ventricular wall, occur when arteries are narrow but patent
Transmural infarcts, what does it involve and when does it occur
involve full thickness of ventricular wall, occur when there is obstruction of a single artery
does myocardial regenerate?
NO, damaged tissue is replaced by scar tissue
1 mm ST segment elevation in 2 contiguous leads is indicative of what?
AMI
Creatinine Phosphokinase (CPK), where is it found?
CK-MM
CK-MB
CK-BB
enzyme found in heart (MB), brain(MM) and skeletal muscle(BB)
LDH1 and LDH 2
enzymes used to detect heart damage
Diagnostic gold standard to detect MI
Troponin 1
Thallium Scans
assess ischemia or necrotic muscle tissue
MUGA scans
to evaluate L ventricular function
what kind of rub do you hear with ischemic pericarditis
pericardial friction rub
cardiac output
amount of blood the heart pumps each minute (L/min)
what does the sympathetic nervous do to the heart rate
increases it
what does the parasympathetic nervous do to the heart rate
decreases it
stroke volume
amount of blood the heart pumps with each beat
cardiac reserve
maximum percentage of increase in cardiac output achieved above normal resting level
aortic impedence
loss of elasticity of aortic wall (this increases with aging)
what happens to the left ventricle with aortic impedance?
the left ventricle must generate higher pressure to get blood through
starlings law
the degree to which the heart muscle can stretch
preload
volume of blood the heart pumps out
after load
the pressure it must generate to pump the blood out of the heart
myocardial contractility and its most important factor in what?
force of contraction
important factor: ventricular performance!!
what happens to the heart according to starlings law with heart failure?
there is an increase in muscle stretch but no increase in force of contraction, (a floppy muscle)
heart compliance
the ease with which the heart relaxes as it fills with blood
what will an echo look like with a patient who has systolic heart failure?
it will have a floppy muscle
How do we prevent the heart muscle from becoming floppy with systolic heart failure?
lower the BP
aortic stenosis and HTN effect on after load
it increases it
what does an increased after load do to the heart?
It increases the workload and oxygen consumption
if myocardial contractility is increased, what happens to amount of blood that is ejected?
its increased
if myocardial contractility is increased, what happens to the systolic ejection fraction?
it increases
if myocardial contractility is increased, what happens to the end systolic volume?
it decreases
if myocardial contractility is decreased, what happens to amount of blood that is ejected?
it decreases
if myocardial contractility is decreased, what happens to the systolic ejection fraction?
it decreases
if myocardial contractility is decreased, what happens to the end systolic volume?
it increases
what is dependent on the concentration of catecholamines in the heart muscle
myocardial contractility
what is the myocardial contractility influenced by?
preload, after load and SNS stimulation
negative inotropic effects on the heart (3) and what do they do to it?
hypoxemia of the heart, hypercapnia of the heart, academia (acidosis) of the heart——IT DEPRESSES THE HEART so it can’t work!
inotropic
agent that affects the heart speed of force of contraction
which stretches more easily and which works under pressure? veins or arteries
veins: stretch
Arteries: work under pressure
stroke volume
amount of blood ejected with each ventricular contraction
End-diastolic volume
total volume in L ventricle at end of filling just prior to contraction
End-systolic volume
total volume in L ventricle at the end of the contraction
EF
percent volume of blood ejected with each ventricle contraction
1 cause of heart failure
atherosclerosis
Ischemic heart disease (CAD), AMI, cardiomyopathy, myocarditis, constrictive pericarditis, congenital heart defects are all causes of what kind of heart failure
Intrinsic
COPD, pulmonary embolism, hyperthyroidism, HTN, AV fistulas, drug toxicities are all causes of what kind of heart failure?
secondary
With heart failure there is a decrease in cardiac output, what compensatory responses do you get with this?
SNS increases HR, kidneys release HR to increase BP, anaerobic metabolism and increased oxygen extraction by peripheral cells
what happens to heart muscle with systolic heart failure
L ventricular muscle is stretched out and floppy
what happens to heart muscle with diastolic heart failure?
muscle hypertrophy (heart muscle is bigger causing a decrease in L ventricular chamber size)
high out put heart failure is which kind of heart failure?
diastolic heart failure
low out put heart failure is which kind heart failure?
systolic heart failure
whats the treatment for low output heart failure or systolic heart failure?
diuretics
Left sided heart failure represents?
failure of the left side of the heart to move blood from the lungs to the circulatory system
causes of left sided heart failure
AMI, systemic HTN, cardiomyopathy, aortic stenosis
Because blood backs up into lungs with left sided heart failure, (backward effect) what can you get from this?
pulmonary edema
because blood is not going to the circulatory system with left sided heart failure (forward effect), what compensatory mechanism kick in?
SV decreases and RAA and SNS kick in to try and get HR and BP up which makes the heart failure worse!
why does SOB and cyanosis occur with pulmonary edema?
because lungs are not able to oxygenate the blood so the blood leaves the lungs without being oxygenated
Right sided heart failure represents?
failure of the right side of the heart to move blood from the circulatory system to the lungs
because right sided heart failure isn’t able to pump blood to lungs, what do you get from this?
it causes peripheral edema and congestion of abdominal organs
1 major cause of right sided heart failure?
left ventricular failure d/t excessive pressures in the pulmonary capillary bed
besides left ventricular failure as the major cause of right sided heart failure, what are other causes of right sided heart failure?
cor pulmonale, COPD, PE, valve disease, Right coronary artery infarct, cardiomyopathy
what major organ is affected with R sided heart failure? and what do you get because of it?
the Liver which causes ascites
s/s right sided HF
JVD, plural effusions, hepatomegaly, hypoalbuminemia, resp symptoms only if have lung disease, dependent edema after first 10 lbs gain
Biventricular heart failure
L to R heart failure
right doesn’t cause left but left can cause right
causes of systolic heart failure
AMI, CAD, valve disease
causes of diastolic heart disease
HTN, COPD, pulmonary HTN, aortic stenosis, pulmonic stenosis
class 1 heart disease
patients don’t have any limitations in physical activity
class 2 heart disease
patients have slight limitations of physical activity
class 3 heart disease
patients have marked limitation of physical activity
class 4 heart disease
patients have unable to carry out physical activity without discomfort
congestive cardiomyopathy
associated with hyperthyriodism, alcoholism, childbirth
restrictive cardiomyopathy
heart becomes infiltrated with abnormal substances causing extensive fibrosis
hypertrophic cardiomyopathy
hypertrophy of septum which causes an obstruction of outflow of blood
myocarditis cardiomyopathy
infection from viruses, inflammation from chemo
Chords tendinae
connect valve leaflets to muscles, help keep leaflets closed under pressure
papillary muscle
extension of the heart muscle that pull valves together to prevent back flow
valvular heart disease
occurs when heart valves can’t fully open or close
grade 1 murmur
soft, heard only under quiet conditions
grade 2 murmur
soft, heard under even noises conditions
grade 3 murmur
easily heard, prominent
grade 4 murmur
loud, associated with a thrill
grade 5 murmur
loud, with stethoscope tilted against chest with thrill
grade 6 murmur
very loud with thrill
diastolic murmurs are only graded to?
grade 4
